The protein encoded by ATP1A2 belongs to the family of P-type cation transport ATPases, and to the subfamily of Na+/K+ -ATPases. Additionally we are shipping ATP1A2 Proteins (6) and ATP1A2 Kits (5) and many more products for this protein.

Data indicate that a second-site mutation distant from Na+ site III increases Na+ affinity, Na(+),K(+)-ATPase (show ATP1A1 Antibodies) activity, and cellular K+ uptake in mutants with the replacement of the aspartate.

genome-wide linkage analysis of the migraine phenotype in 38 families with Rolandic epilepsy; evidence found of linkage to migraine at chromosome 17q12-22 and suggestive evidence at 1q23.1-23.2, centering over the FHM2 locus

Three patients with a proven mutation in the ATP1A2 gene clinically presented without hemiparesis.

The present study provides further evidence on the involvement of ATP1A2 mutations in both migraine and epilepsy, underlying the relevance of genetic analysis in families with a comorbidity of both disorders.

We describe a four-generation Italian family with familial hemiplegic migraine (FHM (show CACNA1A Antibodies)) and epilepsy due to a novel ATP1A2 missense mutation

The ouabain-binding site of either the alpha1 or alpha2 Na,K-ATPase (show ATP1A1 Antibodies) subunit does not play an essential role in the development of DOCA-salt hypertension in a mouse model

Central sodium chloride causes hypertension in mice. The blood pressure response is mediated by the ouabain-like substance in the brain, specifically by its binding to the alpha(2)-isoform of the Na,K-ATPase (show ATP1A1 Antibodies).

Atp1a2 expression in heart and vascular smooth muscle is not essential for regulation of basal systolic blood pressure.

Both protein and mRNA expression of alpha1 and alpha2 isoforms of Na,K-ATPase (show ATP1A1 Antibodies) and NKCC1 (show SLC12A2 Antibodies) in the lateral wall were dramatically reduced following a long-term deafening

The cardiotonic steroid-binding site of the alpha2 Na,K-ATPase (show ATP1A1 Antibodies) plays a role in maintaining normal SBP during pregnancy

The Na,K-ATPase alpha(2) subunit is expressed during development when the t-tubules form. These results suggest that the alpha(2) isoform may serve, in part, a physiological role in the muscle t-tubules.

Na,K-ATPase (show ATP1A1 Antibodies) alpha2 isoform could be important in the modulation of neuronal activity in the neonate

biochemical and biophysical characteristics of the alpha(2)beta(1) isozyme of Na(+)/K(+)-ATPase (show ATP1A1 Antibodies) from caveolae vesicles of pulmonary smooth muscle plasma membrane were studied during solubilization and purification

ATP1A2 Antigen Profile

Protein Summary

The protein encoded by this gene belongs to the family of P-type cation transport ATPases, and to the subfamily of Na+/K+ -ATPases. Na+/K+ -ATPase is an integral membrane protein responsible for establishing and maintaining the electrochemical gradients of Na and K ions across the plasma membrane. These gradients are essential for osmoregulation, for sodium-coupled transport of a variety of organic and inorganic molecules, and for electrical excitability of nerve and muscle. This enzyme is composed of two subunits, a large catalytic subunit (alpha) and a smaller glycoprotein subunit (beta). The catalytic subunit of Na+/K+ -ATPase is encoded by multiple genes. This gene encodes an alpha 2 subunit. Mutations in this gene result in familial basilar or hemiplegic migraines, and in a rare syndrome known as alternating hemiplegia of childhood.